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Genitourinary Case Report 8
Contributor: Jingbo Zhang, M.D. and Manmeen Kaur, M.D.
Date: December 12, 2003

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Patient History

   

  Images
 

 

(Download DICOM files)

Figure 1: Axial T2-weighted Turbo Spin Echo (TSE).
Figure 2: Axial T1-weighted Turbo Spin Echo (TSE).
Figure 3: Axial T1-weighted Turbo Spin Echo (TSE).
Figure 4: Axial T2-weighted Turbo Spin Echo (TSE).
Figure 5: Coronal HASTE of the abdomen and pelvis.

 

 

 

Findings

 

 

Figure 1: Axial T2-weighted TSE image demonstrates a 1 cm midline cystic lesion containing a fluid-debris level in the prostate.

Figure 2: Axial T1-weighted TSE image demonstrates T1 hyperintensity within the midline cystic lesion in the prostate, which is consistent with hemorrhagic or proteinaceous fluid contents.

Figure 3: Axial T1-weighted TSE demonstrates aT1 hyperintense signal within the right seminal vesicle, which is consistent with hemorrhagic or proteinaceous fluid content. The left seminal vesicle is absent. There is a bladder diverticulum in the expected location of the ureterovesicular junction (UVJ).

Figure 4: Axial T2-weighted TSE image demonstrates a low signal intensity in the right seminal vesicle consistent with hemorrhagic or proteinaceous fluid. The left seminal vesicle is absent. The bladder diverticulum is again visualized in the expected location of the UVJ. This diverticulum appears to have a small ureteric bud remnant attached to its lateral surface.

Figure 5: Coronal HASTE image demonstrates an unremarkable right kidney without hydronephrosis. The left kidney is not visualized and is likely congenitally absent.

 

 

 

Diagnosis

 

 

Utricular Cyst. Congenitally absent left kidney and left seminal vesicle.

 

 

 

Discussion

 

 

Hematospermia is a common clinical entity and in most patients this symptom is often overlooked because it is often intermittent and self-limited. However, in some patients, hematospermia may the first indicator of urologic disease. This condition can affect men of any age. Most men with hematospermia are young men (< 40 years of age) and have symptoms ranging in duration from 1-24 months. In these younger patients the etiology of hematospermia is most often benign. In older men, it is rarely associated with malignancy. Most patients have more than one episode, occurring over weeks to months, and the condition often resolves on its own within 1-2 months. While no uniformly accepted definition of chronic hematospermia, blood in the ejaculate that persists for more than 10 ejaculations or hematospermia that persists beyond 2 months requires further evaluation to determine the cause. Hematospermia can be associated with a variety of genital and seminal tract abnormalities including:

  • Primary malignancy: prostate cancer, malignancy of the seminal vesicles.
  • Inflammatory conditions: involving the urethra, prostate or seminal vesicle (e.g., prostatitis, urethritis).
  • Vascular deformity: prostatic telangiectasia and varices.
  • Calculi: prostatic, seminal vesicle.
  • Infection: tuberculosis, HIV, schistosomiasis, cytomegalovirus, hydatid disease (Echinococcus).
  • Congential anomalies: cysts of the prostate and seminal vesicles.
  • Trauma: prostate biopsy, hemorrhoidal sclerosing injection, urethral self-instrumentation,
    testicular and perineal blunt trauma.
  • Systemic disorders: hypertension, chronic liver disease, amyloidosis, lymphoma, and bleeding diatheses (von Willebrand disease).
  • Idiopathic: present in approximately half of the cases.
  • Miscellaneous: calculi (prostatic, seminal vesicle), urethral polyps, and strictures.

MIDLINE PROSTATIC CYSTS

Prostatic cysts are the most commonly encountered congenital anomalies of the prostate and have an incidence of approximately 1% in autopsy specimens. Prostatic cysts are reported in 20% of infertile males with ejaculatory duct obstruction. Prostatic cysts are characterized by their location in relation to the prostate, which may be midline (prostatic utricle and Mullerian duct cysts), paramedian (cysts of the ampulla of the vas deferens and ejaculatory duct), or lateral (seminal vesicle and prostatic cysts). They occur between the prostatic urethra or bladder anteriorly and the rectum posteriorly.

Utricular cysts arise from the dilatation of the prostatic utricle, originating from the verumontanum, and are embryologically of mesodermal and endodermal origin. They communicate freely with the prostatic urethra and contain white or straw-colored sperm-free fluid, which is of high signal on T2-weighted MR images. Utricular cysts are usually smaller than Mullerian duct cysts and are usually 8-10 mm long, teardrop shaped, and do not extend above the base of the prostate. They usually manifest in the first 2 decades of life and are frequently associated with other genital anomalies including hypospadias, cryptorchidism, or ipsilateral renal agenesis.

Mullerian duct cysts are embryologic remnants of the Mullerian duct system and originate entirely from mesoderm. Unlike utriclar cysts, Mullerian duct cysts do not communicate with the prostatic urethra. When large, Mullerian duct cysts can extend superolaterally above the prostate gland and may contain hemorrhage and debris. They are connected to the verumontanum by a stalk. Mullerian duct cysts are rarely associated with renal agenesis. Mullerian duct cysts occur in 4-5% of newborns and in 1% of men. These cysts are usually discovered in infertile males in the 3rd or 4th decade of life because they the most common cause of ejaculatory duct obstruction. They contain sperm-free serous or mucoid, clear brown or green fluid. Stones, which may cause hemorrhage into the cyst, are common and virtually diagnostic if found to lie in a retrovesical cavity that is not connected to the bladder.

With utricular and Mullerian duct cysts, clinical symptoms can range from voiding difficulty to infertility and often overlap between the two cyst types, although most patients are asymptomatic. The clinical features of utricular and Mullerian duct cysts include pelvic mass, obstructive and irritative urinary tract symptoms, hematuria, suprapubic or rectal pain, sexual dysfunction, and symptoms of ejaculatory duct obstruction, such as hematospermia. Urine may pool in utricle cysts since these cysts communicate with the urethra, occasionally resulting in the distinctive feature of postvoid dribbling.

Utricular and Mullerian duct cysts are generally high in signal intensity on T2-weighted MR images secondary to their fluid contents. These cysts demonstrate variable signal intensity on T1-weighted MR images depending on the presence of infection or hemorrhage.

The indication for treatment of these cysts is entirely based on symptoms and does not differ between cyst type. Generally small, asymptomatic, incidentally diagnosed cysts and well-drained cysts are best left alone with periodic follow up. Cysts may rupture spontaneously. Prostatic cysts also have a 3% incidence of malignancy, including clear cell carcninoma, squamous cell carcinoma, and prostatic adenocarcinomas. Complicated and large cysts can be cured with open operation or just aspiration in order to decrease some unavoidable injuries to surrounding structures. Endoscopic unroofing or transurethral incision in the area of the verumontanum should be considered as the first choice of treatment for the most symptomatic cases of prostatic cysts.

SEMINAL VESICAL AGENESIS

The seminal vesicles are paired secretory glands just posterior to the bladder. Congenital anomalies of the seminal vesicles including ectopia, hypoplasia, and agenesis and other internal genital abnormalities are frequently associated. During embryologic development of the genitourinary tract, in the male, involution of the Mullerian ducts results at an adult age in the appendix of the testis and the prostatic utricle.

Unilateral agenesis of the seminal vesicles is thought to result from an embryologic insult before separation of the ureteral bud from the mesonephric ducts, which usually occurs during the 7th week of gestation. Agenesis of the seminal vesicles can be unilateral or bilateral. Bilateral seminal vesicle agenesis is rare. Unilateral agenesis is frequently associated with ipsilateral agenesis of the ductus deferens and with renal agenesis--79% of patients with absence of a seminal vesicle have ipsilateral renal agenesis, 12% had ipsilateral renal abnormalities, and only 9% had normal kidneys bilaterally. The contralateral seminal vesicle is often hypoplastic. It is believed that if the insult occurs after 7 weeks gestation, the seminal vesicle anomaly may not be associated with renal ageneis.

On T2-weighted MR images, the seminal vesicles display high signal intensity that is greater than that of the surrounding fat. Detection of congenital seminal vesicle abnormalities warrants evaluation of the remainder of the genitourinary tract.

References:

  1. Semelka, Richard. Abdominal-Pelvic MRI. New York: Wiley-Liss Inc, 2002. pp. 983-984, 1005.
  2. Cho RI, Lee MS, et al. Magnetic Resonance Imaging in Hemospermia. Clinical Urology. 1997; 157(1): 258-262.
  3. Schiff JD and J Mulhall. Hematospermia (2002). eMedicine (04/19/04).
  4. Zhu JP and HH Meyhoff. Prostatic Cysts: An Unusual But Important Finding in the Male Urogenital Dysfunction. Scandinavian Journal of Urology and Nephrology. 1995; 29: 345-349.
  5. McDermott VG, Meakem III TJ, et al. Prostatic and Periprostatic Cysts: Findings on MR Imaging. American Journal of Roentgenology. 1995; 164: 123-127.
  6. Nghiem HT, Kellman GM, et al. Cystic Lesions of the Prostate. Radiographics. 1990; 10: 635-650.
  7. King BF, Hattery RR, et al. Seminal Vesicle Imaging. RadioGraphics. 1989; 9(4): 653-675.
  8. Dominguez C, Boronat F, et al. Agenesis of Seminal Vesicles in Infertile Males: Ultrasonic Diagnosis. European Urology. 1991; 20: 129-132.
  9. Oh-Oka H, Fujisawa M, et al. Male Genital Malformations Associated With Renal Agenesis. Urology. 2003; 61: 1260xv-1260xvii.
  10. Parsons RB, Fisher AM, et al. MR Imaging in Male Infertility. RadioGraphics. 1997; 17: 627-637.
  11. Trigaux JP, Van Beers B, et al. Male Genital Tract Malformations Associated with Ipsilateral Renal Agenesis: Sonographic Findings. Journal of Clinical Ultrasound. 1991; 19: 3-10.

 

 

 
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